ArticlePLoS neglected tropical diseases2019
Shortening of Zika virus CD-loop reduces neurovirulence while preserving antigenicity.
Article in PLoS neglected tropical diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Fisetin limits Chikungunya virus-induced apoptosis hallmarks in hepatocellular carcinoma cells.Scientific reports · 2025Article
- Identification of a Zika NS2B epitope as a biomarker for severe clinical phenotypes.RSC medicinal chemistry · 2021Article
- Identifying crucial E-protein residues responsible for unusual stability of Zika virus envelope.Biophysical journal · 2021Article
- Compound Porcine Cerebroside and Ganglioside Injection (CPCGI) Attenuates Sevoflurane-Induced Nerve Cell Injury by Regulating the Phosphorylation of p38 MAP Kinase (p38MAPK)/Nuclear Factor kappa B (NF-κB) Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Role of Zika Virus Envelope Protein Domain III as a Target of Human Neutralizing Antibodies.mBio · 2019Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Zika virus (ZIKV) is a mosquito-borne positive sense RNA virus. Recently, ZIKV emerged into the Western hemisphere as a human health threat, with severe disease associated with developmental and neurological complications. The structural envelope protein of ZIKV and other neurotropic flaviviruses contains an extended CD-loop relative to non-neurotropic flaviviruses, and has been shown to augment ZIKV stability and pathogenesis. Here we show that shortening the CD-loop in ZIKV attenuates the virus in mice, by reducing the ability to invade and replicate in the central nervous system. The CD-loop mutation was genetically stable following infection in mice, though secondary site mutations arise adjacent to the CD-loop. Importantly, while shortening of the CD-loop attenuates the virus, the CD-loop mutant maintains antigenicity in immunocompetent mice, eliciting an antibody response that similarly neutralizes both the mutant and wildtype ZIKV. These findings suggest that the extended CD-loop in ZIKV is a determinant of neurotropism and may be a target in live-attenuated vaccine design, for not only ZIKV, but for other neurotropic flaviviruses.
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